E. coli O157:H7 Season is Nearly Upon Us – Will it be 2005 and 2006 or 2007 and 2008?

The presence of E. coli O157:H7 in hamburger was defined as an adulterant under the Federal Meat Inspection Act in 1994. However, recalls of E. coli O157:H7 contaminated meat and related illnesses continued over the next decade to grow, as did my law firm. Oddly too, and with near regularity, E. coli O157:H7 recalls and illnesses seemed to begin in the Spring and peak in late Summer and Fall from 1993 through 2002.

After 24 million pounds of contaminated beef were recalled in 34 separate incidents in 2002, recalls dropped off to just over a million pounds a year for the next three years, and then to just 181,900 pounds in 2006. The Centers of Disease Control and Prevention saw E. coli O157:H7 – related illnesses drop 48% between 2000 and 2006.

The reality is that from 1993 through 2002, children sickened with E. coli O157:H7 tainted hamburger made up the bulk of my law practice. However, as E. coli O157:H7 hamburger recalls fell from 2003 through the end of 2006, I wondered if the law firm would survive. Springs just simply were not the same.

But then came Spring 2007. E. coli O157:H7, which begins its life in the hindgut of a cow, mounted a surge on its home court. And, it came back with a vengeance. Since the Spring of 2007, forty-four million pounds of beef have been recalled in 25 incidents due to E. coli O157:H7. And, I am now back in the meat business, and look to Spring not just for the beginning of hay fever season.

Now, Spring 2009 is upon us. In preparing for it, I had some research done on the “seasonality” of E. coli O157:H7 in both humans and cattle and then say what was available in the literature as to the reasons behind it. Perhaps it does not fully explain what I experienced from 1993 though 2008, but it is a start. It is all about being prepared.

Seasonality in humans:

• A review of E. coli O157:H7 diarrhea in the US by Slutsker et al (1997) found that E. coli O157:H7 was isolated most frequently from patients during the summer months.
• Results from an epidemiological review of E. coli O157:H7 outbreaks in the US (1982-2002) showed that outbreaks involving ground beef peaked in summer months (Rangel et al, 2005)
• In a review of non-O157 STEC infections in the US from 1983-2002 revealed that these infections also were most frequent during the summer (Brooks et al, 2005)
• In Scotland, HUS and E. coli O157:H7 infections peaked in patients under 15 years of age in July/August, followed by a plateau from June to September (Douglas et al, 1997). Interestingly, the prevalence in Scottish beef cattle at slaughter was found to be highest during the winter, but the concentration of E. coli O157:H7 (number of bacteria shed in cattle feces) was highest during the warmer months (Ogden et al, 2004).

Seasonality in ruminants:

• Numerous studies in cattle indicate that fecal shedding of E. coli O157:H7 is typically low in the winter, increases in the spring, peaks during the summer and tapers off in the fall (Edrington et al, 2006; Hancock et al, 2001; Hussein et al, 2005, etc.)
• Barkocy-Gallagher et al (2003) found that the prevalence of E. coli O157:H7 in cattle feces peaked in the summer, and prevalence on hides (a known risk factor for beef contamination) was highest from spring through fall.
• A survey of ground beef samples in the US showed that they were 3x more likely to be contaminated with E. coli O157:H7 from June – September (Chapman, et al 2001)
• A survey in the UK found that the majority of retail meats that tested positive for E. coli O157:H7 were collected between May and September.

Hypotheses on why there are seasonal differences in prevalence in both humans and cattle

• Speculation that temperature may affect shedding or survival in feces (warmer months promoting survival and/or growth of E. coli O157:H7).
• Studies by Edrington et al (2006 and 2008) suggested that day length and effects on hormones such as melatonin secretion from the gastrointestinal tracts may be the underlying mechanism for seasonality in cattle. The authors hypothesized that the seasonal variation is a result of physiological responses within the host animal to changing day-length. Hormones have been shown to play a role in the regulation of bacterial populations and host immunity.